Abstract
Nitric oxide (NO) and prostanoids induce coronary vasodilation directly, but also indirectly by modulating endothelin (ET)‐mediated vasoconstriction. We have shown that ET‐induced coronary vasoconstriction disappears after myocardial infarction (MI). We aimed to investigate the interactions between NO, prostanoids and ET in control of coronary tone after MI.Changes in coronary tone in response to ETAB blockade with Tezosentan alone and following inhibition of eNOS (LNNA) or cyclooxygenase (Indomethacin) were measured in chronically instrumented swine (27 normal; 14 MI), at rest and during exercise (EX).In normal swine, LNNA and Indo caused coronary vasoconstriction (decrease in cvSO2) at rest and during EX and increased the vasodilator effect of tezosentan, particularly during EX.In swine with MI, the vasoconstrictor effect of LNNA was decreased. A vasodilator effect of tezosentan was uncovered after LNNA, however this effect was decreased as compared to normal swine. Indo‐induced vasoconstriction was maintained after MI, while a vasodilator effect of tezosentan was unmasked at rest and during EX. This effect was increased compared to normal swine.Our results show that both NO and prostanoids exert their vasodilator influence on the coronary vasculature at least in part through suppression of the endogenous ET system, particularly after MI.Supported by Netherlands Heart Foundation (2000T042)
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